AuthorYubeta, Isabella Bella
MetadataShow full item record
PublisherThe University of Arizona.
RightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
AbstractDiabetic retinopathy (DR) affects approximately 93 million people worldwide (Yau et al., 2012) and is a leading cause of blindness among adults aged 20-74 years in the United States (Fong et al., 2004). DR is a complication of diabetes that occurs when the integrity of the blood vessels in the retina slowly become damaged due to many long-term factors including hyperglycemia (Morgan et al., 2016). Although pericyte loss is commonly observed as one of the earliest morphological changes, the timeframe and mechanisms leading to the development of DR are not yet fully understood. Treatment for DR remains limited and is unable to reverse early damage or vision loss. The density of pericytes within all three retinal vascular layers has not been extensively investigated at a time when deficits in retinal neuronal pathways have been previously observed. To determine if pericyte cells exhibit caspase-3, a marker of apoptosis, and the density of pericyte coverage among the retinal vascular layers, whole-mounted-retinas from 6-weeks-post-STZ-treated and control mice were imaged. The average number of pericytes per micron length of vessel is significantly reduced in diabetes, however there is no statistically significant difference in expression of caspase-3 to suggest that this is due to apoptosis.
Degree ProgramHonors College